Evidence map›Paper›PMID 27080257›Full record

ArticleThe Journal of biological chemistry2016

Intermedin Restores Hyperhomocysteinemia-induced Macrophage Polarization and Improves Insulin Resistance in Mice.

Yanli Pang, Yang Li, Ying Lv, Lulu Sun, Songyang Zhang, Yin Li, Yuhui Wang, George Liu, Ming-Jiang Xu, Xian Wang and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.4field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Integrated Omics RevealPharmaceuticals (Basel, Switzerland) · 2025
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  14. Homocysteine regulates fatty acid and lipid metabolism in yeast.The Journal of biological chemistry · 2018
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Yanli PangFrom the Department of Physiology and Pathophysiology, Basic Medical College, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, and Center for Reproductive Medicine of Third Hospital, Peking University, Beijing 100191, China.
Yang LiFrom the Department of Physiology and Pathophysiology, Basic Medical College, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, and.
Ying LvFrom the Department of Physiology and Pathophysiology, Basic Medical College, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, and.
Lulu SunFrom the Department of Physiology and Pathophysiology, Basic Medical College, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, and.
Songyang ZhangFrom the Department of Physiology and Pathophysiology, Basic Medical College, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, and.
Yin LiFrom the Department of Physiology and Pathophysiology, Basic Medical College, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, and.
Yuhui WangFrom the Department of Physiology and Pathophysiology, Basic Medical College, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, and.
George LiuFrom the Department of Physiology and Pathophysiology, Basic Medical College, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, and.
Ming-Jiang XuFrom the Department of Physiology and Pathophysiology, Basic Medical College, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, and.
Xian WangFrom the Department of Physiology and Pathophysiology, Basic Medical College, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, and xwang@bjmu.edu.cn.
Changtao JiangFrom the Department of Physiology and Pathophysiology, Basic Medical College, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, and jiangchangtao@bjmu.edu.cn.
Ministry of Education of the People's Republic of China · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperhomocysteinemia (HHcy) is a condition characterized by an abnormally high level of homocysteine, an inflammatory factor. This condition has been suggested to promote insulin resistance. To date, the underlying molecular mechanism remains largely unknown, and identifying novel therapeutic targets for HHcy-induced insulin resistance is of high priority. It is well known that intermedin (IMD), a calcitonin family peptide, exerts potent anti-inflammatory effects. In this study, the effects of IMD on HHcy-induced insulin resistance were investigated. Glucose tolerance and insulin tolerance tests were performed on mice treated with IMD by minipump implantation (318 ng/kg/h for 4 weeks) or adipocyte-specific IMD overexpression mice (Adipo-IMD transgenic mice). The expression of genes and proteins related to M1/M2 macrophages and endoplasmic reticulum stress (ERS) was evaluated in adipose tissues or cells. The expression of IMD was identified to be lower in the plasma and adipose tissues of HHcy mice. In both IMD treatment by minipump implantation and Adipo-IMD transgenic mice, IMD reversed HHcy-induced insulin resistance, as revealed by glucose tolerance and insulin tolerance tests. Further mechanistic study revealed that IMD reversed the Hcy-elevated ratio of M1/M2 macrophages by inhibiting AMP-activated protein kinase activity. Adipo-IMD transgenic mice displayed reduced ERS and lower inflammation in adipose tissues with HHcy. Soluble factors from Hcy-treated macrophages induced adipocyte ERS, which was reversed by IMD treatment. These findings revealed that IMD treatment restores the M1/M2 balance, inhibits chronic inflammation in adipose tissues, and improves systemic insulin sensitivity of HHcy mice.

Indexed as

Adipose TissueAMP-Activated Protein KinasesAnimalsBlotting, WesternCells, CulturedEndoplasmic Reticulum StressHyperhomocysteinemiaInflammationInsulin ResistanceMacrophage ActivationMacrophages, PeritonealMaleMice, Inbred C57BLMice, TransgenicNeuropeptidesReverse Transcriptase Polymerase Chain ReactionAMP-Activated Protein Kinasesintermedin protein, mouseNeuropeptidesadipose tissueAMP-activated kinase (AMPK)homocysteineinsulin resistancemacrophage

Identifiers

PMID27080257
PMCPMC4933280
OpenAlexW2336241590

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.